Theme 3: Lecture 12 - Heart failure Flashcards
1
Q
Definition of heart failure
A
A state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body
2
Q
What is heart failure a result of
A
Results from any structural or functional abnormality that impairs the ability of the ventricle to eject blood (systolic HF) or fill with blood (diastolic HF)
3
Q
What affects stoke volume
A
- contractility
- preload
- afterload
4
Q
In general, what does an increased heart rate result in
A
increased cardiac output
5
Q
What does an excessively high heart rate result in
A
decrease in the amount of time allowed for the ventricles to fill in diastole which causes stroke volume and, thus cardiac output to fall
6
Q
What is the typical cardiac output at rest
A
70mls/kg/min
7
Q
What is contractility
A
the intrinsic ability of the myocardium to contract
8
Q
What is preload
A
the volume of blood or stretching of cardiomyocytes at the end of diastole prior to the next contraction
9
Q
What is afterload
A
- the resistance/end load against which the ventricle contracts to eject blood
- It is the pressure in the aorta/pulmonary artery that the left/right ventricular muscle must overcome to eject blood
10
Q
What affects preload
A
- Is affected by venous blood pressure and the rate of venous return to the heart
- This, in turn, is affected by venous tone and volume of circulating blood
11
Q
What causes an increase in preload
A
Preload increases with increasing blood volume and vasoconstriction
12
Q
What causes a decrease in preload
A
Preload decreases with blood volume loss and vasodilatation
13
Q
Describe the Frank Starling law
A
- An increase in volume of blood filling the heart stretches the heart muscle fibres causing greater contractile forces which, in turn, increases the stroke volume
- Is true only up to a certain point… at some stage the fibres become over-stretched and the force of contraction is reduced
14
Q
What causes an increase in afterload
A
- The greater the aortic/pulmonary pressure, the greater the afterload on the left/right ventricle respectively
- Afterload increase with hypertension and vasoconstriction
15
Q
How does afterload affect cardiac output
A
As afterload increases, cardiac output decreases
16
Q
Low output heart failure
A
- Systolic heart failure
- Diastolic heart failure
17
Q
High output heart failure
A
- Occurs in the context of other medical conditions which increase demands on cardiac output, causing a clinical picture of HF
- The heart itself is functioning normally but cannot keep up with the unusually high demand for blood to one or more organs in the body
18
Q
Which medical conditions cause high output heart failure (6)
A
- thyrotoxicosis
- profound anaemia
- pregnancy
- pagets disease
- acromegaly
- sepsis
19
Q
What is thyrotoxicosis
A
overactive thyroid gland
20
Q
What is Paget’s disease
A
Paget’s disease of bone is a chronic disease of the skeleton. In healthy bone, a process called remodeling removes old pieces of bone and replaces them with new, fresh bone. Paget’s disease causes this process to shift out of balance, resulting in new bone that is abnormally shaped, weak, and brittle.
21
Q
What is acromegaly
A
Acromegaly is a disorder that results from excess growth hormone (GH) after the growth plates have closed. The initial symptom is typically enlargement of the hands and feet. There may also be an enlargement of the forehead, jaw, and nose
22
Q
What is systolic heart failure
A
Progressive deterioration myocardial contractile function
23
Q
What causes systolic heart failure
A
- Ischaemic injury
- Volume overload
- Pressure overload
24
Q
What is diastolic heart failure
A
Inability of the heart chamber to relax, expand and fill sufficiently during diastole to accommodate an adequate blood volume
25
What causes diastolic heart failure
- Significant left ventricular hypertrophy (LVH) e.g HCM
- Infiltrative disorders
- Constrictive pericarditis
- Restrictive cardiomyopathy
26
What are the causes of heart failure
- Coronary Heart Disease
- Hypertensive Heart Disease
- Valvular Heart Disease
- Myocardial Disease/ Cardiomyopathies
- Congenital Heart Disease
27
Definition of cardiomyopathies
Diffuse disease of the heart muscle leading to functional impairment
28
What are the classes of cardiomyopathies
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
29
Causes of dilated cardiomyopathy
- various causes, 50% familial
- ETOH
- pregnancy
- systemic disease (SLE)
- muscular dystrophies
- Drug toxicity
- Myocarditis
30
What is myocarditis
Inflammation of the myocardium (heart muscle)
31
What are muscular dystrophies
Muscular dystrophy is a group of inherited diseases that damage and weaken your muscles over time.
32
Causes of hypertrophic cardiac myopathy
hereditary
33
Causes of restrictive cardiomyopathy
rare-amyloid the main cause in the UK
34
What is amyloid
A glycoprotein that is deposited in internal organs in amyloidosis
35
Describe the pathophysiology of heart failure
Pump failure leads to reduced SV and CO. Compensatory mechanisms kick in to maintain arterial pressure and perfusion of vital organs:
The Frank Starling mechanism: vasoconstriction, increased venous return to the heart, increased preload, heart muscle fibres stretch, enhanced contractility (initially beneficial but there is a limit beyond which this becomes unhelpful)
Myocardial structural change: Augmented muscle mass (hypertrophy) with or without cardiac chamber dilatation
Activation of neurohormonal system:
- Release of Noradrenaline – increases heart rate and myocardial contractility. Causes vasoconstriction
- Release of ANP/BNP
- Activation of renin-angiotensin – aldosterone system
36
Describe the NP system
- Distended ventricular wall leads to release of proBNP
- proBNP is converted into either BNP or NT-proBNP
- BNP is active and leads to diuresis, RAAS inhibition, SNS inhibition and vasodilation
- NT-proBNP in non active but is used as a biomarker for heart failure
37
What does NP stand for
Natriuretic peptide
38
What does activation of the NP system lead to
- Decreased BP
- Decreased sympathetic tone
- Decreased aldosterone levels
- Natriuresis
- Diuresis
- Antifibrotic affects
39
Describe what vasoconstriction does as a compensatory mechanism in heart failure
↑ resistance against which heart has to pump (i.e.↑afterload), and may therefore ↓ CO
40
Describe what Na+ and water retention does an a compensatory mechanism in heart failure
↑fluid volume, which ↑ preload. If too much “stretch” → ↓ contractile strength and CO
41
Describe what excessive tachycardia does as a compensatory mechanism in heart failure
↓diastolic filling time → ↓ventricular filling → ↓SV and CO
42
What are the clinical types of heart failure
- Left sided, right sided and biventricular failure
- Acute and chronic heart failure
- Compensated and decompensated heart failure
43
What does left sided heart failure do
Backs up progressively from the left atrium to the pulmonary circulation
44
Causes of left sided heart failure
- Ischaemic heart disease
- Hypertension
- Valvular heart disease
- Myocardial disease
45
The symptoms of left sided heart failure due to the effect on the lungs
- Pressure in the pulmonary veins is transmitted retrogradely to the capillaries and arteries
- This leads to pulmonary congestion and oedema
- Heavy wet lungs:
- Breathlessness (dyspnoea) exaggeration of the normal breathlessness that follows exertion
- Orthopnoea – breathlessness lying flat that is relieved by sitting or standing
- Paroxysmal nocturnal dyspnoea – an extension of orthopnoea with attacks of extreme dyspnoea bordering on suffocation usually occuring at night
46
The symptoms of left sided heart failure due to effect on the kidneys
- Decreased cardiac output
- Reduction in renal perfusion
- Activation of renin - angiotensin – aldosterone system
- Retention of salt and water with consequent expansion of interstitial fluid and blood volumes
47
The symptoms of left sided heart failure due to effect on the brain
- Hypoxic encephalopathy (brain disease/damage)
- Irritability
- Loss of attention
- Restlessness
- Stupor and coma
48
Causes of right sided heart failure
- Usually as a consequence of left sided heart failure (congestive cardiac failure (CCF))
- Cor-pulmonale
- Valvular heart disease
- Congenital heart disease
49
What is core pulmonale
- Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
- Usually as a result of respiratory disease e.g. COPD or pulmonary emboli
- Normal left ventricular function
50
Symptoms of right sided heart failure due to effect on the liver and portal system
- Congestive hepatomegaly (enlarged liver)
- Centrilobular necrosis when severe
- Cardiac cirrhosis
51
Symptoms of right sided heart failure do to the effect on the spleen
Congestive splenomegaly (enlargement of the spleen)
52
Symptoms of right sided heart failure do to effect on the abdomen
Ascites
53
Symptoms of right sided heart failure do to effect on the subcutaneous tissue
- Peripheral oedema of dependent portions of the body esp. ankle and pretibial oedema
- Sacral oedema if bedridden
54
Symptoms of right sided heart failure do to effect on the pleural and pericardial space
effusions
55
What causes biventricular heart failure (congestive cardiac failure)
-Either due to the same pathological process on each side of the heart
OR
-A consequence of left heart failure leading to volume overload of the pulmonary circulation and eventually the right ventricle causing right ventricular failure
56
Clinical presentation on heart failure due to fluid accumulation
- Dyspnoea
- Orthopnoea, paroxysmal nocturnal dyspnoea
- Oedema
- Hepatic congestion
- Ascites
57
Clinical presentation of heart failure due to reduction in cardiac output
- Fatigue
| - Weakness
58
New York Heart Association (NYHA) classification of heart failure
- Class I: No limitation of physical activity
- Class II: Slight limitation of ordinary activity
- Class III: Marked limitation, even during less-than-ordinary activity
- Class IV: Severe limitation with symptoms at rest
59
Clinical signs of heart failure (9)
- Cool, pale, cyanotic extremities
- Tachycardia
- Elevated JVP
- Third heart sound (S3) – gallop rhythm
- Displaced apex (LV enlargement)
- Crackles or decreased breath sounds at bases on chest auscultation
- Peripheral oedema
- Ascites
- Hepatomegaly
60
Clinical tests for heart failure
- CXR
- ECG
- Blood investigations
- Echocardiogram / Cardiac MRI or CT / CT-PET
- CTCA (CT coronary angiography) / Coronary angiography
61
Name a loop diuretic
Frusemide
62
Describe loop diuretics
- Inhibit Na+ re-absorption from the proximal tubule
- K+ loss from distal tubule
- Can be given iv or orally
63
Side effects of loop diuretics
- electrolyte abnormalities
| - hypovolaemia and diminished renal perfusion
64
What is hypovolaemia
abnormally low extracellular fluid volume
65
Name a mineralocorticoid receptor antagonist
Spironolactone
66
Describe mineralocorticoid receptor antagonists (aldosterone antagonists)
- antagonizes the action of aldosterone at mineralocorticoid receptors
- Acts on distal tubule
- Promotes Na+ excretion and K+ re-absorption
- Reduces hypertrophy and fibrosis
67
Side effects of mineralocorticoid receptor antagonists (aldosterone antagonists)
- Gynaecomastia (esp. Spironolactone)
| - Electrolyte (K+ high) and renal function abnormalities
68
What is gynaecomastia
males develop breast tissue
69
Name an ACE inhibitor
Ramipril
70
Describe ACE inhibitors
- Act on activated renin - angiotensin system
- Given orally in small doses with slow titration
- Block production of angiotensin:
- Vasodilatation
- BP lowering
- Reduce cardiac work
71
Side effects of ACE inhibitors
- Cough
- Hypotension
- Renal impairment
72
Name a beta blocker
bisoprolol
73
Describe beta blockers
- Block the action of adrenaline and noradrenaline on adrenergic beta receptors
- Slow HR, reduce BP
- Given orally in small doses with slow titration
- (treat arrhythmias)
74
Side effects of beta blockers
- Bronchospasm
| - Claudication
75
What is claudication
pain and/or cramping in the lower leg due to inadequate blood flow to the muscles
76
Name an SA node blocker
Ivabradine
77
Describe ivabradine
- Blocks the If channel within the SA node
- Slow HR, no effect on BP
- Given orally with dose titration
78
Side effects of ivabradine
- Visual aura
| - Bradycardia
79
Describe digoxin
- Increases myocardial contractility
- Slows conduction at the AV node (use in AF)
- Excreted by kidney - Toxicity important
80
When is digoxin given
- Acute HF especially in AF
| - Chronic HF in selected cases
81
Describe Angiotensin receptor neprilysin inhibitors (ARNI)
- Acts on activated renin - angiotensin system
- Also blocks breakdown of ANP/BNP
- Block production of angiotensin: (Vasodilatation, BP lowering, reduce cardiac work)
- Promote natriuresis: (Sodium excretion, vasodilatation, reduce hypertrophy and fibrosis)
82
Side effects of Angiotensin receptor neprilysin inhibitors
- Hypotension
| - Renal impairment
83
What is neprilysin
A protein that breaks NPs down into inactive fragments among other things
84
Non drug therapies for heart failure (7)
- Cardiac Resynchronisation Therapy (CRT)
- Implantable Cardioverter Defibrillator (ICD)
- Dialysis & Ultrafiltration
- Ventricular Assist Device (LVAD/RVAD)
- Intra-aortic balloon pump
- Cardiac transplantation
- (Stem cell therapy)
85
Describe cardiac resynchronisation therapy AKA biventricular pacing
- Standard pacemakers equipped with two wires (or "leads") conduct pacing signals to specific regions of heart
- Biventricular pacemakers have an additional third lead designed to conduct signals directly into the left ventricle
- Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.
